Cholinergic Agonists
High-yield Verified · Oct 2026Raise cholinergic signalling two ways — by binding muscarinic receptors directly (Gq → calcium in smooth muscle and glands, Gi → slowing in the heart) or by blocking acetylcholinesterase, so acetylcholine builds up at muscarinic, ganglionic and neuromuscular synapses.
Nursing view → administration, monitoring and patient teaching
Compare: Autonomic receptors compared — muscarinic, nicotinic, adrenergic and dopamine →
Drugs
* Anticholium (physostigmine): Not FDA-approved. A German product imported under a temporary importation license to address a US shortage.
Mechanism
Direct agonists (bethanechol, pilocarpine, methacholine, carbachol, cevimeline) stimulate muscarinic receptors; indirect agonists (neostigmine, pyridostigmine, physostigmine; echothiophate irreversibly) inhibit acetylcholinesterase, increasing synaptic acetylcholine at muscarinic and neuromuscular-junction nicotinic receptors.
Muscarinic receptors and their second messengers
Acetylcholine acts on muscarinic (M1–M5) and nicotinic (Nm, Nn) receptors. M1 receptors sit on gastric parietal cells and in the CNS, M2 receptors in the heart, and M3 receptors on smooth muscle, exocrine glands and the bladder; nicotinic receptors are in the CNS, adrenal medulla, autonomic ganglia and the neuromuscular junction.
M1, M3 and M5 couple to Gq: phospholipase C cleaves PIP2 into IP3 and DAG, IP3 releases stored calcium, and the rise in intracellular calcium contracts smooth muscle and drives exocrine secretion. In intestinal, bladder, airway and eye smooth muscle, calcium–calmodulin activates myosin light chain kinase and the muscle contracts.
M2 and M4 couple to Gi, which inhibits adenylyl cyclase and lowers cAMP. M2 is the predominant receptor of the SA and AV nodes: its activation lets potassium out, hyperpolarizing the nodal cells, so heart rate and atrial contractility fall.
Blood vessels are the exception: muscarinic agonists dilate them. Calcium in endothelial cells activates nitric oxide synthase, NO diffuses into the underlying smooth muscle and raises cGMP, and the muscle relaxes; where the endothelium is damaged and makes no NO, acetylcholine contracts the vessel instead.
Direct agonists: choline esters and alkaloids
The direct agonists bind and activate muscarinic receptors themselves. They come in two chemical families: the choline esters (acetylcholine, methacholine, carbachol, bethanechol) and the alkaloids (muscarine, pilocarpine, cevimeline). Unlike acetylcholine — which cholinesterase hydrolyzes so fast that its effects are transient — the therapeutic agonists resist the enzyme: bethanechol is not destroyed by cholinesterase, so its effects last longer.
Bethanechol is selective for muscarinic receptors: in therapeutic oral or subcutaneous doses nicotinic effects are usually absent or minimal, the doses that stimulate micturition and defecation do not ordinarily stimulate ganglia or voluntary muscle, and its charged quaternary amine keeps it out of the brain. It contracts the detrusor strongly enough to empty the bladder.
The others are chosen by where they act. Pilocarpine contracts the ciliary muscle — tension on the scleral spur opens the trabecular meshwork and aqueous outflow rises — and constricts the iris sphincter; given orally it stimulates the salivary, sweat and other exocrine glands, as does cevimeline. Carbachol constricts the iris and ciliary body and is placed inside the eye for miosis during surgery. Inhaled methacholine constricts bronchial smooth muscle, which has significant parasympathetic (cholinergic) innervation; hyperreactive airways respond to smaller doses, which is the basis of the challenge test.
Acetylcholinesterase and the indirect agonists
Acetylcholinesterase ends cholinergic transmission: acetylcholine is not taken back up but hydrolyzed into choline and acetate in the cleft, and the choline is recaptured to make more transmitter. The enzyme has two active sites — an anionic site (tryptophan) and an esteratic site (serine). Butyrylcholinesterase (plasma cholinesterase) is a second enzyme, found in plasma and organs such as the liver.
Cholinesterase inhibitors protect acetylcholine from hydrolysis and raise both its level and its duration of action. The reversible inhibitors — neostigmine, pyridostigmine, physostigmine and the Alzheimer drugs — are the ones used therapeutically (StatPearls groups the reversible class as carbamates). The irreversible ones are the organophosphates: insecticides such as parathion and malathion, nerve agents such as sarin and soman, and the eye drop echothiophate. Organophosphates inactivate the enzyme by phosphorylating the serine hydroxyl of the esteratic site.
Where the drug goes depends on its charge. Neostigmine is a water-soluble, ionized quaternary ammonium compound that does not penetrate the blood–brain barrier, and pyridostigmine is also quaternary; both act mainly at peripheral synapses and the neuromuscular junction. Physostigmine, like the organophosphates, has more marked muscarinic and CNS effects and less prominent action on skeletal muscle — the reason it reverses the central effects of anticholinergic poisoning.
The neuromuscular junction, myasthenia and the two crises
At the motor end plate, cholinesterase inhibitors raise acetylcholine so that more of it activates the postsynaptic receptors — the basis of their use in myasthenia gravis, an autoimmune disease with antibodies against the acetylcholine receptor (or, in another form, against muscle-specific tyrosine kinase, MuSK). Nicotinic receptors are ligand-gated ion channels. Pyridostigmine, the usual first-line inhibitor, differs from neostigmine in its longer duration of action and fewer gastrointestinal side effects.
Too much drug turns help into harm. After an anticholinesterase, acetylcholine released by a nerve impulse can make skeletal muscle fire repetitively (twitching, fasciculations), and higher doses block neuromuscular transmission, producing weakness or paralysis. This is the cholinergic crisis: increasing weakness that can reach the respiratory muscles, usually with muscarinic signs.
A myasthenic crisis — the disease itself worsening, triggered for example by infection, surgery or drugs that impair neuromuscular function such as some antibiotics (e.g. gentamicin) — also produces extreme weakness, and the two can be hard to tell apart; patients may pass from one to the other without a visible change. Their treatments are opposite: myasthenic crisis calls for more intensive anticholinesterase therapy, cholinergic crisis for prompt withdrawal of these drugs and atropine. The bedside edrophonium (Tensilon) test once separated them — strength improved in myasthenic crisis and worsened in cholinergic crisis — but edrophonium has been discontinued and is no longer available in the United States.
Comparing the drugs
Direct muscarinic agonists
| Drug | Chemical family | Route | Labeled use | Distinguishing point |
|---|---|---|---|---|
| Bethanechol | Choline ester | Oral | Nonobstructive urinary retention; neurogenic atony of the bladder | Not destroyed by cholinesterase; muscarinic-selective; quaternary — does not cross the blood–brain barrier |
| Pilocarpine | Alkaloid | Eye drops; oral tablets | Open-angle glaucoma or ocular hypertension (drops); dry mouth after head-and-neck radiotherapy or in Sjögren syndrome (tablets) | Ciliary-muscle contraction opens the trabecular meshwork; oral half-life about 0.8–1.4 h |
| Cevimeline | Alkaloid | Oral | Dry mouth in Sjögren syndrome | CYP2D6 and CYP3A3/4 metabolism; half-life about 5 h |
| Carbachol | Choline ester | Intraocular; eye drops (with brimonidine) | Miosis during surgery; presbyopia (with brimonidine) | Constricts the iris and ciliary body |
| Methacholine | Choline ester | Inhaled | Diagnosis of bronchial airway hyperreactivity (challenge test) | Boxed warning: severe bronchoconstriction |
Every direct agonist acts at muscarinic receptors; which tissue it reaches depends on the product and route.
Cholinesterase inhibitors
| Drug | Inhibition | Reaches the CNS? | Route | Use | Elimination and half-life |
|---|---|---|---|---|---|
| Neostigmine | Reversible (competitive) | No — quaternary ammonium | IV, IM or SC | Reversal of nondepolarizing neuromuscular blockade | Hydrolysis by cholinesterase and hepatic microsomal metabolism; renal excretion; half-life 24–113 min, longer in renal dysfunction |
| Pyridostigmine | Reversible | No — quaternary amine | Oral (also parenteral) | Myasthenia gravis | Mainly excreted unchanged by the kidney; half-life about 3 h |
| Physostigmine | Reversible | Yes — marked CNS effects | IV | Central effects of anticholinergic poisoning | Rapid hydrolysis by plasma esterases; half-life about 20–30 min |
| Echothiophate | Irreversible (organophosphate), long-acting | — | Eye drops | Elevated intraocular pressure; accommodative esotropia | Absorbed enough to depress plasma and red-cell cholinesterase after a few weeks of use |
Reversible inhibitors release the enzyme; organophosphates phosphorylate it. — = not described in the listed sources.
Pharmacokinetics
- Resistance to cholinesterase — bethanechol and the other direct agonists
- Acetylcholine itself is rapidly hydrolyzed by cholinesterase, so its effects are transient. Bethanechol is not destroyed by cholinesterase, which is why its effects outlast acetylcholine’s; direct agonists in general resist acetylcholinesterase.
- Charge and the blood–brain barrier — bethanechol, neostigmine, pyridostigmine, physostigmine
- Bethanechol’s charged quaternary amine keeps it from crossing the blood–brain barrier, and quaternary neostigmine and pyridostigmine do not cross it either. Physostigmine, in contrast, has marked CNS effects.
- Onset and duration — bethanechol
- Oral effects on the GI and urinary tracts sometimes appear within 30 minutes but more often take 60 to 90 minutes to peak, and usually last about an hour; subcutaneous injection acts within 5 to 15 minutes and more intensely on the bladder. Its metabolism and excretion have not been elucidated.
- Renal elimination — pyridostigmine, neostigmine
- Pyridostigmine is poorly absorbed orally (10%–20%), mainly excreted unchanged by the kidney (75%–81%), and has a half-life of about 3 hours, so lower doses may be needed in renal disease. Neostigmine is primarily excreted renally; its elimination half-life of 24–113 minutes lengthens with renal dysfunction (about 181 minutes in anephric patients).
- Ester hydrolysis — physostigmine
- Rapidly hydrolyzed by plasma esterases, with a half-life of about 20–30 minutes; it is cleared within about 2 hours. Its short action means anticholinergic signs can recur, and the label allows the effective dose to be repeated if they do.
- CYP metabolism — cevimeline
- Metabolized by CYP2D6 and CYP3A3/4, mostly to sulfoxide and glucuronide metabolites; the mean half-life is about 5 hours and 84% of a dose is excreted in urine within 24 hours. Food slows its absorption. Drugs that inhibit CYP2D6 or CYP3A3/4 slow its metabolism.
- Systemic absorption from the eye — echothiophate, pilocarpine, carbachol
- Echothiophate drops depress both plasma and red-cell cholinesterase in most patients after a few weeks. Pilocarpine drops reach measurable plasma levels at steady state, and carbachol and brimonidine were quantifiable in plasma in fewer than half of subjects after a dose of the combination drops.
- No data — methacholine
- The label has no metabolic or pharmacokinetic data for inhaled methacholine.
Pharmacogenomics
Uses & drug choice
- Urinary retention / neurogenic bladder & postoperative ileus (bethanechol, neostigmine)
- Myasthenia gravis (pyridostigmine, neostigmine); reversal of non-depolarizing NMB (neostigmine)
- Glaucoma and dry mouth/eyes (pilocarpine)
- Cevimeline for dry mouth in Sjögren syndrome
- Carbachol placed inside the eye for miosis during surgery and to reduce the pressure rise in the first 24 hours after cataract surgery; carbachol with brimonidine (Yuvezzi eye drops) for presbyopia
- Methacholine (inhaled) for the methacholine challenge test — diagnosing airway hyperreactivity in people without clinically apparent asthma
- Physostigmine, given IV and not FDA-approved, to reverse the central nervous system effects of anticholinergic poisoning
- Echothiophate eye drops for elevated intraocular pressure and accommodative esotropia
Adverse effects
- Salivation, sweating and lacrimation
- Gland secretion is driven through M3 (and M2) receptors. Sweating is the odd one out: sweat glands are sympathetic, but their postganglionic receptors are muscarinic, so cholinergic drugs cause diaphoresis.
- Abdominal cramping, diarrhea, urinary urgency
- M3-mediated smooth-muscle contraction: gastrointestinal tone and peristalsis rise while sphincters relax, and the detrusor contracts while the trigone and sphincter relax, emptying the bladder.
- Miosis, blurred or dim vision
- The iris sphincter contracts (miosis) and the ciliary muscle contracts (spasm of accommodation). Miotics can therefore cause accommodative spasm and temporary dim or dark vision.
- Bradycardia, AV block and hypotension
- M2 activation hyperpolarizes SA nodal cells (bradycardia, even arrest) and slows conduction at the AV node and Purkinje fibers, up to complete block. M3 receptors on vessels mediate dilation through endothelial nitric oxide, so blood pressure falls and the skin flushes.
- Bronchospasm and bronchorrhea
- M3 stimulation constricts bronchial smooth muscle and increases tracheobronchial secretions. Airways that are already hyperreactive constrict at lower doses — exactly what the methacholine test exploits, and why the test itself can trigger severe bronchoconstriction.
- Fasciculations and weakness (cholinesterase inhibitors)
- Excess acetylcholine at the neuromuscular junction makes muscle fire repetitively (fasciculations); at higher doses the end plate stays depolarized and transmission fails — a depolarizing block that causes weakness or flaccid paralysis.
- Seizures and CNS effects (physostigmine)
- Physostigmine acts in the brain, where cholinergic drugs produce stimulation followed by depression; excess central acetylcholine can cause seizures and coma. Given too quickly, it also causes bradycardia and hypersalivation.
Toxicity & antidote
Organophosphates — esters formed from phosphoric acid and an alcohol, absorbed through the lungs, gut, eyes and skin — inhibit acetylcholinesterase, and acetylcholine floods muscarinic, nicotinic and central synapses. Muscarinic excess gives miosis, bradycardia, bronchospasm, bronchorrhea, salivation, lacrimation, urination, diarrhea and emesis (sweating comes through the sympathetic muscarinic supply). Nicotinic excess gives fasciculations progressing to flaccid paralysis through a depolarizing block, and — through sympathetic ganglia and the adrenal — sometimes mydriasis, tachycardia and hypertension. CNS excess brings seizures and coma. Death is usually from respiratory failure: bronchoconstriction, bronchorrhea, central respiratory depression and respiratory-muscle weakness.
The organophosphate phosphorylates the enzyme’s serine. That bond can still be reversed — spontaneous regeneration is slow, taking hours to days — but with time the enzyme ages: the bond becomes irreversible, and function returns only as new enzyme is synthesized. Pralidoxime binds the organophosphate and reactivates the phosphorylated enzyme (mainly outside the CNS), and it slows aging; it therefore works only before aging, whose time course depends on the compound. Its most critical effect is relieving respiratory-muscle paralysis, the nicotinic effect atropine cannot touch. It is less effective against central respiratory depression, so atropine — which competes with acetylcholine at muscarinic receptors — is always given with it, and is given first.
Several traps follow from the mechanism. Succinylcholine is avoided for intubation because it cannot be metabolized and paralysis is prolonged. After the cholinergic crisis has ended, an intermediate syndrome of proximal and neck-flexor weakness and cranial-nerve palsies can follow at 24–96 hours and progress to respiratory failure without cholinergic signs, and lipophilic compounds released from fat can bring the cholinergic signs back. Pralidoxime is not indicated for carbamate insecticides (it may increase carbaryl toxicity), nor for poisoning by phosphorus or organophosphates without anticholinesterase activity. Red-cell acetylcholinesterase activity is thought to track the clinical picture better than plasma butyrylcholinesterase.
Interactions
Contraindications
- Asthma (bethanechol: latent or active asthma; oral pilocarpine and cevimeline: uncontrolled asthma; physostigmine: asthma) — Labeled contraindication — cholinergic stimulation causes bronchospasm and increased secretions.
- COPD, or asthma with neostigmine, pyridostigmine or echothiophate use caution — Cholinergic stimulation causes bronchospasm and increased secretions — a labeled caution rather than a listed contraindication for these products.
- Mechanical GI or urinary obstruction (bethanechol, neostigmine, pyridostigmine, physostigmine) — Labeled contraindication — stimulating contraction against a blockage risks perforation (bethanechol is for nonobstructive retention).
- Bethanechol with hyperthyroidism, peptic ulcer, pronounced bradycardia or hypotension, or coronary artery disease — Labeled contraindications — added vagal tone slows the heart further, increases acid, and can trigger arrhythmia in hyperthyroidism.
- Bethanechol with epilepsy, parkinsonism, vasomotor instability, marked vagotonia, or hypersensitivity to the drug — Labeled contraindications for bethanechol.
- Bethanechol after recent bladder surgery or bowel resection/anastomosis, or with peritonitis, acute GI inflammation, spastic GI disturbances, bladder-neck obstruction, or a weakened bladder or bowel wall — Labeled contraindications — stronger bladder and gut contractions could harm a healing, inflamed, or weakened wall.
- Neostigmine or pyridostigmine with bradycardia, cardiac conduction disease, or peptic ulcer disease use caution — Added vagal tone slows the heart further and increases acid — a caution rather than a listed contraindication for these drugs.
- Oral pilocarpine (Salagen) or cevimeline with acute iritis, narrow-angle glaucoma, or hypersensitivity to the drug — Labeled contraindications — the drug constricts the pupil, which is harmful in these eye conditions.
- Methacholine with baseline FEV1 below 60% of predicted (or below 1.5 L in adults), or hypersensitivity to methacholine or other parasympathomimetic drugs — Labeled contraindications (low lung function is also in the boxed warning) — the challenge test can cause severe bronchoconstriction.
- Methacholine challenge with clinically apparent asthma or wheezing, uncontrolled hypertension, aortic aneurysm, a history of myocardial infarction or stroke, or pregnancy use caution — The label does not recommend the test in these settings (in pregnancy because of possible fetal hypoxia); epilepsy, vagotonia, peptic ulcer, thyroid disease or urinary obstruction call for a benefit–risk judgment first.
- Physostigmine with asthma, gangrene, diabetes, cardiovascular or coronary disease, mechanical bowel or urinary obstruction, a vagotonic state, myotonic dystrophy, or closed traumatic brain injury — Labeled contraindications for physostigmine.
- Physostigmine with succinylcholine or another depolarizing neuromuscular blocker, with choline esters, or in poisoning with irreversible cholinesterase inhibitors (organophosphates) or barbiturates — Labeled contraindications — physostigmine can deepen a depolarizing block and worsen paralysis, and other cholinesterase inhibitors add to its cholinergic effects.
- Echothiophate with active uveal inflammation, most angle-closure glaucoma without an iridectomy, or hypersensitivity — Labeled contraindications — the drug can increase angle block and can activate latent iritis or uveitis.
- Echothiophate with marked vagotonia, asthma, spastic GI disturbances, peptic ulcer, pronounced bradycardia and hypotension, recent myocardial infarction, epilepsy, parkinsonism, or a prior retinal detachment use caution — Label precautions — to be used with caution, if at all, where vagotonic effects could cause harm.
- Intraocular carbachol (Miostat) with acute heart failure, asthma, peptic ulcer, hyperthyroidism, GI spasm, urinary tract obstruction, or Parkinson disease use caution — Label cautions; its only listed contraindication is hypersensitivity (the vial stopper also contains natural rubber latex).
- Cevimeline with cardiovascular disease (angina or prior myocardial infarction), controlled asthma or COPD, or kidney or gallbladder stones use caution — Label warnings — it can alter heart rate and conduction, raise airway resistance and secretions, and contract biliary and ureteral smooth muscle (cholecystitis, biliary obstruction, renal colic).
High-yield
- Neostigmine — quaternary ammonium: does not penetrate the blood–brain barrier
- Pyridostigmine — quaternary amine: does not cross it either
- Physostigmine — the one with marked CNS effects: reverses central anticholinergic poisoning
Bethanechol, a direct agonist, is quaternary too and stays out of the brain.
- Reactivate — pralidoxime frees the phosphorylated enzyme and relieves respiratory-muscle paralysis
- Before — it works only before aging, whose timing depends on the compound
- Ages — aged enzyme is irreversibly inhibited; recovery needs new enzyme
Atropine is still given — first — for the muscarinic effects, and pralidoxime is not indicated for carbamate insecticides.
Practice questions
Q1A 41-year-old farmworker is brought in after spraying an organophosphate insecticide in a closed shed. He has pinpoint pupils, drooling, wheezing with copious bronchial secretions, a heart rate of 44/min and diffuse muscle fasciculations. After repeated IV atropine his secretions dry and his heart rate rises, but his respiratory muscles keep weakening.
Which drug, given as early as possible, best addresses the remaining weakness?
- A.More atropine
- B.Glycopyrrolate
- C.Physostigmine
- D.Pralidoxime
- E.Neostigmine
Show answer
D. Pralidoxime — Organophosphates phosphorylate acetylcholinesterase, flooding muscarinic and nicotinic synapses. Atropine competes only at muscarinic receptors and does not mitigate nicotinic effects, so neuromuscular weakness persists. Pralidoxime reactivates the phosphorylated enzyme — its most critical effect is relieving respiratory-muscle paralysis — but only before the enzyme ages. Glycopyrrolate is another antimuscarinic, and physostigmine and neostigmine are cholinesterase inhibitors that would add to the excess.
Q2A 33-year-old woman with myasthenia gravis increased her own pyridostigmine doses over several days because of fatigue. She now has worsening weakness with difficulty swallowing, plus abdominal cramps, diarrhea, sweating, small pupils and fasciculations.
Which is the most appropriate next step?
- A.Withdraw the cholinesterase inhibitor and give atropine, with breathing support as needed
- B.Increase pyridostigmine to overcome the weakness
- C.Add neostigmine for a faster effect
- D.Add bethanechol to strengthen the muscles
- E.Give physostigmine
Show answer
A. Withdraw the cholinesterase inhibitor and give atropine, with breathing support as needed — Muscarinic signs and fasciculations with rising weakness after dose escalation point to a cholinergic crisis: excess acetylcholine at the end plate blocks transmission. Myasthenic crisis is treated with more anticholinesterase, but cholinergic crisis calls for prompt withdrawal of these drugs and atropine; supportive care such as mechanical ventilation may be needed. Adding neostigmine or physostigmine would deepen the crisis, and bethanechol acts selectively at muscarinic receptors and does not ordinarily stimulate voluntary muscle.
Q3A 26-year-old man has episodic cough and chest tightness, but his baseline spirometry is normal. He inhales increasing concentrations of methacholine while his FEV1 is measured, and the test is stopped when FEV1 falls by 22%.
The test drug narrowed his airways by which mechanism?
- A.Blocking β2 receptors on bronchial smooth muscle
- B.Releasing histamine from mast cells
- C.Inhibiting acetylcholinesterase in the airways
- D.Stimulating Gi-coupled M2 receptors that raise cAMP
- E.Stimulating Gq-coupled muscarinic receptors on airway smooth muscle, raising intracellular calcium
Show answer
E. Stimulating Gq-coupled muscarinic receptors on airway smooth muscle, raising intracellular calcium — This is a methacholine challenge: a fall in FEV1 of 20% or more is a positive test, and hyperreactive airways constrict at lower doses. Methacholine, a choline ester, agonizes airway muscarinic receptors; M3 receptors couple to Gq, phospholipase C and IP3, and the calcium rise contracts smooth muscle. It does not block β2 receptors or inhibit cholinesterase, and M2/Gi receptors lower — not raise — cAMP.
Q4A 7-year-old boy who uses echothiophate eye drops for accommodative esotropia has general anesthesia for a tonsillectomy. After intubation with succinylcholine, he does not breathe spontaneously for far longer than expected.
Which best explains the prolonged paralysis?
- A.Echothiophate blocked nicotinic receptors at the end plate
- B.Systemic cholinesterase inhibition from the drops prolonged the action of succinylcholine
- C.Echothiophate is a short-acting reversible inhibitor whose effect had worn off
- D.Echothiophate stimulated muscarinic receptors on the diaphragm
- E.Succinylcholine reactivated the phosphorylated enzyme
Show answer
B. Systemic cholinesterase inhibition from the drops prolonged the action of succinylcholine — Echothiophate is a long-acting organophosphate cholinesterase inhibitor, and the drops depress both plasma and red-cell cholinesterase in most patients after a few weeks. Prolonged paralysis has been reported when succinylcholine is given with drugs that have anticholinesterase activity, so in these patients it is given only with great caution, if at all, because of possible respiratory or cardiovascular collapse. Echothiophate inhibits the enzyme rather than blocking receptors, skeletal muscle signals through nicotinic (not muscarinic) receptors at the neuromuscular junction, and reactivation is pralidoxime’s action.
Q5A 58-year-old woman cannot void two days after a hysterectomy; a catheter drains a large volume and imaging shows no obstruction. The team wants a drug that will contract the detrusor without nicotinic or central effects.
Which property makes bethanechol suitable where acetylcholine itself would not be?
- A.It inhibits acetylcholinesterase in the bladder wall
- B.It is a tertiary amine that reaches the sacral spinal cord
- C.It is not destroyed by cholinesterase and acts selectively at muscarinic receptors
- D.It is a nicotinic agonist at autonomic ganglia
- E.It blocks M2 receptors on the detrusor
Show answer
C. It is not destroyed by cholinesterase and acts selectively at muscarinic receptors — Acetylcholine is rapidly hydrolyzed by cholinesterase, so its effects are transient. Bethanechol is not destroyed by the enzyme, its action is selective for muscarinic receptors (nicotinic effects are usually absent or minimal at therapeutic doses), and its charged quaternary amine keeps it out of the brain. It contracts the detrusor and is indicated only for nonobstructive retention — mechanical obstruction is a contraindication.
Sources
- Cholinergic Medications — direct/indirect agonists, uses, adverse effects — StatPearls (NCBI)
- Cholinergic Crisis — SLUDGE, bradycardia/bronchospasm, atropine — StatPearls (NCBI)
- Bethanechol Chloride Tablets — nonobstructive urinary retention; contraindications incl. asthma, bradycardia, peptic ulcer, hyperthyroidism, obstruction (FDA label) — FDA / DailyMed
- Salagen (pilocarpine) Tablets — dry mouth; contraindicated in uncontrolled asthma (FDA label) — FDA / DailyMed
- Pilocarpine Ophthalmic Solution — glaucoma; ciliary-muscle mechanism (FDA label) — FDA / DailyMed
- Neostigmine Methylsulfate Injection — NMB reversal; bradycardia, obstruction contraindication, cholinergic crisis (FDA label) — FDA / DailyMed
- Mestinon (pyridostigmine) — myasthenia gravis; cholinergic vs myasthenic crisis (FDA label) — FDA / DailyMed
- Bethanechol — indications, empty-stomach dosing, adverse effects — StatPearls (NCBI)
- Neostigmine — uses, overdose and cholinergic crisis — StatPearls (NCBI)
- Myasthenia Gravis — pyridostigmine as symptomatic therapy — StatPearls (NCBI)
- Organophosphate Toxicity — cholinergic toxidrome, atropine and pralidoxime — StatPearls (NCBI)
- Muscarinic Agonists — bethanechol and neostigmine for ileus and urinary retention; pilocarpine in glaucoma — StatPearls (NCBI)
- Parasympathomimetic Medications — indications, adverse effects, hyperthyroidism and atrial fibrillation — StatPearls (NCBI)
- Autonomic Pharmacology — cholinomimetic uses and adverse effects — StatPearls (NCBI)
- Intestinal Pseudo-Obstruction — neostigmine and the perforation risk in true obstruction — StatPearls (NCBI)
- Physiology, Autonomic Nervous System — parasympathetic “rest and digest” — StatPearls (NCBI)
- Anticholium (physostigmine) — antidote for the anticholinergic syndrome; unapproved shortage import; contraindications, slow IV, atropine at hand (DailyMed label) — FDA / DailyMed
- Cholinesterase Inhibitors — physostigmine use, interactions and contraindications — StatPearls (NCBI)
- Provocholine (methacholine) — methacholine challenge test; boxed warning: severe bronchoconstriction (FDA label) — FDA / DailyMed
- Miostat (carbachol intraocular solution) — miosis during surgery; cautions, latex stopper (FDA label) — FDA / DailyMed
- Yuvezzi (carbachol and brimonidine) eye drops — presbyopia; miotic vision and retinal-detachment warnings (FDA label) — FDA / DailyMed
- Evoxac (cevimeline) — dry mouth in Sjögren syndrome; contraindications, warnings, interactions (FDA label) — FDA / DailyMed
- Phospholine Iodide (echothiophate) — elevated IOP and accommodative esotropia; succinylcholine and insecticide warnings (FDA label) — FDA / DailyMed
- Regonol (pyridostigmine injection) — drug interactions: antibiotics that intensify neuromuscular block, quinidine (FDA label) — FDA / DailyMed
- Pyridostigmine bromide tablets (Amneal) — drug interactions: neuromuscular blockers, aminoglycosides, opioids (FDA label) — FDA / DailyMed
- Protopam (pralidoxime) — reactivation of phosphorylated cholinesterase, aging, carbamate warning (FDA label) — FDA / DailyMed
- Table of Pharmacogenomic Biomarkers in Drug Labeling (cevimeline: CYP2D6) — U.S. Food and Drug Administration
By LearnDrugs
Educational summary for medical students. Always verify against current prescribing information and guidelines. Not medical advice.